Affiliations: Department of Physiology, Akdeniz University Faculty of Medicine, Antalya, Turkey | Department of Nuclear Medicine, Akdeniz University Faculty of Medicine, Antalya, Turkey | Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
Note: [] Corresponding author: Oguz K. Baskurt, Department of Physiology, Akdeniz University Faculty of Medicine, Kampus, Antalya 07070, Turkey. Tel.: +90 242 310 1560; Fax: +90 242 310 1561; E-mail: [email protected].
Abstract: It is well known that the hematocrit in microvessels with diameters smaller than 1000 μm is lower than either venous or arterial hematocrit, thereby resulting in significantly lower mean hematocrit values for vessels perfusing a given tissue (i.e., lower tissue hematocrit). The mechanisms that underlie this reduction of microvascular hematocrit include axial migration, plasma skimming and the Fahraeus Effect. It has been previously demonstrated in rats that a linear hematocrit gradient normally exists through the thickness of the left ventricular myocardium, and that this gradient is sensitive to alterations of the rheological properties of the circulating blood. The gradient is abolished if the RBC in the perfusate are rigid; fibrinogen infusions, and thus increases of both plasma viscosity and RBC aggregation, also affect this gradient. In a new series of studies, it has been observed that enhanced RBC aggregation affects the myocardial hematocrit gradient regardless of alterations of plasma viscosity. Although the exact mechanisms responsible for the myocardial hematocrit gradient, as well as its physiological significance, are not yet clearly known, it is possible to speculate that alterations in local hematocrit could adversely affect myocardial perfusion and function.
